This is an unprogrammed cell death. It is death of the cell or group of cells that are still part of the living organism. It is also referred to as premature cell death. This type of cell death is caused by factors external to the cells or tissues e.g. toxins and infections; Necrosis is almost always detrimental and can be fatal. Necrosis typically begins with cells swelling, chromatin digestion and disruption of the plasma membranes and organelle membranes.
TYPES OF NECROSIS
There are seven distinctive morphological patterns of necrosis.
1. Coagulative necrosis
It is a form of a tissue death in which the component cells are dead but the basic architecture is preserved for at least several days. The affected tissue takes a firm texture. Coagulative necrosis is typically seen in hypoxic environment such as infarction. The cell outline remaining after cell death can be observed by light microscopy. Coagulative necrosis can be caused by ischemia. Ischemia results in decreased ATP, increased cytosolic Ca2+ and free radical formation which eventually cause membrane damage. Decreased ATP causes decreased action of Na+ K+ pumping into the cell membrane leading to increased Na+ and water in the cells.
2. Liquefactive necrosis/Colliquative necrosis.
This is usually caused by focal bacterial infection because they can attract polymorphonuclear leucocytes. The enzymes in the polymorphs are released to fight the bacteria but also dissolve the tissues nearby causing an accumulation of pus effectively liquefying the tissues e.g abscess.
3. Caseous Necrosis
Most commonly encountered in foci in TB infection. The term caseous (cheese like) is derived from the friable yellow to white appearance of the area of necrosis.
Unlike coagulative necrosis, the tissue architecture is completely obliterated and cellular outline can’t be discerned. Caseous necrosis is often enclosed within a distinctive informatory border. This appearance is characteristic of a focus of inflammation known as granuloma.
Results from action of lipase on fatty tissues e.g acute pancreatitis and breast tissue necrosis.
There are two types of fat necrosis (a) Enzymatic fat necrosis
(b)Traumatic fat neucrosis
The effect of enzyme lipase is to release free acid which can combine with Ca2+ to produce soapy deposits in the tissues.
Histologically one sees shadowing outlines of fat cells (like coagulative necrosis) but with Ca2+ deposits form cells and surrounding inflammatory reactions.
This is a special form of necrosis usually seen in immune reactions involving blood vessels. Its caused by immune mediated vascular damage. This results from the deposition of antigen and antibody complexes in the walls of arteries.
This type of necrosis is restricted to spirocheatal infections e.g syphilis infections.
This is due to blockage of various drainage of an organ/tissue e.g testicular torsion- testicle twists on the cord that provides its blood supply.
Table 1–1 Features of Necrosis and Apoptosis
Feature Necrosis Apoptosis
Cell size Enlarged (swelling) Reduced (shrinkage)
Pyknosis → karyorrhexis → karyolysis Fragmentation into nucleosome-size fragments
Plasma membrane Disrupted Intact; altered structure, especially orientation of lipids
Cellular contents Enzymatic digestion; may leak out of cell Intact; may be released in apoptotic bodies
Adjacent inflammation Frequent No
Physiologic or pathologic role Invariably pathologic (culmination of irreversible cell injury) Often physiologic, means of eliminating unwanted cells; may be pathologic after some forms of
cell injury, especially DNA damage